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Biomedical subjects

E Lowenstein

Publications and source records attributed to E Lowenstein.

At least 19 recordsLinked to original sources
PubMed2000

The effect of heparin-coated pulmonary artery catheters on activated coagulation time in cardiac surgical patients.

OBJECTIVE: To investigate the effect of heparin-coated pulmonary artery catheters (HPACs) on activated coagulation time (ACT) drawn through a non-heparin-coated introducer sheath. DESIGN: A prospective, observational study. SETTING: University teaching hospital. PARTICIPANTS: Patients scheduled for surgical procedures requiring cardiopulmonary bypass. INTERVENTIONS: With institutional review board approval, 63 patients without prior coagulopathy undergoing procedures requiring cardiopulmonary bypass were studied. Jugular venous and radial arterial ACTs were measured before and immediately after insertion of an HPAC. Additional measurements were obtained 1 hour later and 4 minutes after completion of protamine infusion. MEASUREMENTS AND MAIN RESULTS: The ACT drawn from the introducer after placement of an HPAC was 48 seconds greater than the ACT drawn before the HPAC was placed (p < 0.0001). This difference was still present 1 hour later but not after the administration of protamine or in blood drawn at any time from another site. Baseline ACTs drawn from radial arterial catheters, kept patent using a heparin flush system, resulted in elevated measurements, despite withdrawing seven times the deadspace before taking a sample. CONCLUSIONS: Blood obtained from an introducer with an HPAC in situ provides a spuriously high ACT. ACTs drawn from catheters kept patent using heparin flush also result in prolonged measurements. Baseline ACT measurement from an introducer should be obtained before placement of the HPAC.

Adult↗
PubMed1999

Effect of sevoflurane and desflurane on the myogenic constriction and flow-induced dilation in rat coronary arterioles.

BACKGROUND: Determinants of myocardial blood flow distribution include metabolic, myogenic, endothelial, and neurohumoral control mechanisms. The authors studied the effect of sevoflurane and desflurane on the myogenic and endothelial mechanisms. METHODS: Wistar rat subepicardial microvessels, approximately 100 microm in diameter, were monitored for diameter changes in vitro using a video detection system. Myogenic vasomotion was studied by varying the intraluminal pressure from 10 mmHg to 120 mmHg. Flow-induced, endothelium-dependent dilation was evaluated in U46619-preconstricted vessels by varying the pressure gradient across the isolated vessel from 10 mmHg to 80 mmHg, while maintaining the midpoint luminal pressure constant at 40 mmHg to avoid myogenic effects. Myogenic and flow-induced vasomotion both were studied in the presence of sevoflurane, 1 or 2 minimum alveolar concentration (MAC) (MAC is a unit of inhalational anesthetic potency), desflurane, 1 or 2 MAC, or no anesthetic (control). RESULTS: Myogenic constriction was shown above intraluminal pressures of 70 mmHg. Myogenic constriction was unchanged by sevoflurane, 1 MAC (P = 0.24), but was mildly enhanced by sevoflurane, 2 MAC (P < 0.05), or desflurane, 1 (P < 0.05) or 2 MAC (P < 0.01). Flow-induced dilation was shown over the pressure gradient range of 10-80 mmHg. Flow-induced dilation was not altered significantly by sevoflurane, 1 or 2 MAC (P > 0.3 each), but was significantly attenuated by desflurane, 1 or 2 MAC (P < 0.001 each). CONCLUSIONS: Sevoflurane maintains myogenic and endothelial determinants of myocardial blood flow distribution. Conversely, desflurane attenuates endothelium-dependent flow-induced dilation while mildly enhancing myogenic constriction.

Anesthetics, Inhalation↗
PubMed1999

Incorporating palliative care into critical care education: principles, challenges, and opportunities.

OBJECTIVE: To identify the goals and methods for medical education about end-of-life care in the intensive care unit (ICU). DATA SOURCES AND STUDY SELECTION: A status report on palliative care, a summary report of recent research on palliative care education, articles in the medical literature on end-of-life care and critical care, and expert opinion were considered. DATA EXTRACTION: A working group, including specialists in critical care, palliative care, medical ethics, consumer advocacy, and communications, was convened at the "Medical Education for Care Near the End of Life National Consensus Conference." A modified nominal group process was used to develop a consensus. DATA SYNTHESIS: In the ICU, life and death decisions are often made in a crisis mode or in the face of uncertainty, and may necessitate the withholding and withdrawal of life-supporting technologies. Because critical illness often diminishes the capacity of patients to make decisions, clinicians must often make decisions in conjunction with surrogates, rather than with patients. Discontinuity of care can threaten trusting relationships, and cultural diversity can have a particularly powerful impact on choices for care. In the face of these realities, it is possible and appropriate to give compassionate palliative care to dying patients and their families in the ICU. CONCLUSIONS: Teaching care of the dying in the ICU should emphasize the following: a) the goals of care should guide the use of technology; b) understanding of prognostication and treatment withholding and withdrawal is essential; c) effective communication and trusting relationships are crucial to good care; d) cultural differences should be acknowledged and respected; and e) the delivery of excellent palliative care is appropriate and necessary when patients die in the ICU.

Attitude to Death↗
PubMed1998

Epithelial dependence of the bronchodilatory effect of sevoflurane and desflurane in rat distal bronchi.

UNLABELLED: The bronchial epithelium releases substances that enhance bronchodilation in response to certain bronchodilators. We examined the hypothesis that the bronchodilatory effect of desflurane and sevoflurane depends on the epithelium in rat distal bronchial segments. Wistar rat subsegmental bronchial segments (diameter approximately 100 microm) were dissected. After preconstriction with 5-hydroxytryptamine, each segment was exposed to increasing concentrations of desflurane 0%-12% or sevoflurane 0%-4.8% under four conditions: after epithelial rubbing, after pretreatment with the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (L-NNA), after pretreatment with the cyclooxygenase inhibitor indomethacin, or with no preintervention (control). Changes in bronchial diameter were monitored using an in vitro video detection system. Both desflurane and sevoflurane produced concentration-dependent bronchodilation (P < 0.001 for either anesthetic; 54% +/- 8% [mean +/- SD] dilation for 12% desflurane and 48% +/- 14% dilation for 4.8% sevoflurane). For both anesthetics, bronchodilation was significantly attenuated by epithelial rubbing (15% +/- 4% dilation for 12% desflurane and 13% +/- 10% dilation for 4.8% sevoflurane; P < 0.001 each), by pretreatment with indomethacin (12% +/- 3% dilation for 12% desflurane and 9% +/- 5% dilation for 4.8% sevoflurane; P < 0.001 each), and by L-NNA (24% +/- 8% dilation for 12% desflurane, P < 0.001; and 17% +/- 10% dilation for 4.8% sevoflurane, P < 0.01). Desflurane- and sevoflurane-mediated bronchodilation depends at least partially on the epithelium, and may involve both a prostanoid and NO in rat distal bronchi. IMPLICATIONS: Bronchodilation by the volatile anesthetics desflurane and sevoflurane is at least partially epithelium-dependent and may be attenuated in diseases affecting the epithelium, such as asthma.

Anesthetics, Inhalation↗
PubMed1998

Flow-induced dilation of rat coronary microvessels is attenuated by isoflurane but enhanced by halothane.

BACKGROUND: Volatile anesthetics attenuate agonist-induced endothelium-dependent vasodilation of coronary arteries. This study considered the hypothesis that the anesthetics may also attenuate flow-induced endothelium-dependent vasodilation. METHODS: Rat subepicardial arteries of approximately 100 microm were monitored for diameter changes in vitro by a video detection system, with the midpoint luminal pressure held constant at 40 mmHg but the pressure gradient (and therefore flow) across each vessel increased from 0 to 80 mmHg, in the presence or absence of 1 or 2 minimum alveolar concentration (MAC) isoflurane or 1 or 2 MAC halothane, with or without 10 microM of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) or 10 microM of the cyclooxygenase inhibitor indomethacin. RESULTS: Flow-induced dilation was attenuated by L-NNA or indomethacin (p < 0.001 each). It was attenuated by isoflurane in a concentration-dependent manner (P < 0.001). Attenuation by 2 MAC isoflurane persisted even in the presence of L-NNA (P < 0.01) or indomethacin (P < 0.05). On the other hand, flow-induced dilation was enhanced by 2 MAC halothane (P < 0.05). Halothane at 1 MAC had no significant effect. Enhancement by 2 MAC halothane was evident in the presence of indomethacin (P < 0.05) but not L-NNA (P = 0.40). CONCLUSIONS: In rat subepicardial arteries, flow-induced dilation is endothelium-dependent and mediated by both NO and a prostanoid. Isoflurane attenuates flow-induced dilation, possibly by decreasing synthesis, the action of NO and a prostanoid, or both, whereas halothane enhances it, possibly by increasing synthesis, the action of NO, or both.

Anesthetics, Inhalation↗
PubMed1997

Isoflurane and halothane attenuate endothelium-dependent vasodilation in rat coronary microvessels.

Volatile anesthetics attenuate endothelium-dependent vasodilation but the mechanism of attenuation remains controversial. The present study examines the mechanism of isoflurane- and halothane-mediated attenuation of endothelium-dependent vasodilation in Wistar rat coronary microvessels of about 100 microns internal diameter. The vessels were studied in vitro in a pressurized (40 mm Hg), no-flow state using video microscopy. After preconstriction of the vessels with the thromboxane analog U46619 1 microM, concentration response curves to acetylcholine (ACh), the calcium ionophore A23187, sodium nitroprusside (SNP), or the stable cyclic guanosine monophosphate (cGMP) analog 8-bromo-cGMP (Br-cGMP) were obtained in the presence of 0% (control), 1% or 2% isoflurane, or 1% or 2% halothane. Isoflurane 1% and 2% significantly attenuated vasodilation to ACh and A23187. Isoflurane 2%, but not 1%, attenuated vasodilation to SNP. Vasodilation to Br-cGMP was not affected by isoflurane. Halothane attenuated vasodilation to ACh, but had no effect on vasodilation to A23187, SNP, or Br-cGMP. We conclude that isoflurane attenuates endothelium-dependent vasodilation by impairing at least two distinct steps in the nitric oxide (NO)-cGMP pathway, the first being between endothelial increase of calcium and smooth muscle guanylate cyclase and the second being inhibition of soluble guanylate cyclase activity. These two steps appear to have different sensitivities to the effect of isoflurane. Halothane has an effect at the endothelial receptor level, but not any distal steps in the NO-cGMP pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

The direct vasomotor effect of thyroid hormones on rat skeletal muscle resistance arteries.

UNLABELLED: The present study examines the hypothesis that the hormones have direct vasodilatory effects and attempts to determine whether the effects are endothelium-dependent. Rat skeletal muscle resistance arteries of approximately 100 microns were dissected, and vessel diameter changes were monitored using a videodetection system. After equilibration at 37 degrees C, each vessel was preconstricted with the thromboxane analog U46619 1 microM, and the percentage of dilation was measured after exposure to increasing concentrations of triiodothyronine (T3) or levothyroxine (T4) (10(-10) to 10(-7) M). Dilation in response to T3 was also measured after endothelial denudation and pretreatment with the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA) 10 microM, the cyclooxygenase inhibitor indomethacin 10 microM, the adenosine triphosphate-sensitive K+ channel blocker glibenclamide 1 microM, or the beta-adrenergic antagonist propranolol 1 microM. Both T3 and T4 demonstrated concentration-dependent dilation of the U46619-preconstricted vessels (P < 0.001 each), with T3 having a greater effect than T4 (P < 0.05) (36% +/- 9% [mean +/- SD] dilation at 10(-7) M T3 vs 24% +/- 6% dilation at 10(-7) M T4). In comparison, isoproterenol 10(-7) M produced 56% +/- 6% dilation. T3-mediated vasodilation was attenuated but not abolished by endothelial denudation (18% +/- 3% dilation at 10(-7) M T3) (P < 0.01), L-NNA (15% +/- 7% dilation at 10(-7) M T3) (P < 0.01), indomethacin (20% +/- 9% dilation at 10(-7) M T3) (P < 0.05), and glibenclamide (22% +/- 7% dilation at 10(-7) M T3) (P < 0.01), but it was not affected by propranolol (37% +/- 20% dilation at 10(-7) M T3) (P = 0.99). We conclude that thyroid hormones possess direct vasodilatory effects with both endothelium-independent and endothelium-dependent components. IMPLICATIONS: Thyroid hormones may have modest direct vasodilatory effects. This may partially account for the cardiovascular actions of the hormones in hyperthyroidism or when administered pharmacologically in cardiac surgery.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Isoflurane- and halothane-mediated dilation of distal bronchi in the rat depends on the epithelium.

BACKGROUND: Respiratory epithelium releases substance(s) that can modulate bronchoconstriction in response to constrictive agonists and enhance bronchodilation in response to certain bronchodilators. The hypothesis that the bronchodilatory effect of isoflurane and halothane depends on the epithelium was tested in rat distal bronchial segments. METHODS: Wistar rat bronchial segments of the fourth order (diameter approximately 100 microns) were dissected. After preconstriction with 5-hydroxytryptamine, each bronchial segment was exposed to increasing concentrations of 0% to 3% isoflurane or 0% to 3% halothane under four conditions: after epithelial rubbing, after pretreatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine, after pretreatment with the cyclooxygenase inhibitor indomethacin, or with no preintervention (control). Changes in bronchial diameter were monitored using an in vitro video detection system. RESULTS: Both isoflurane and halothane produced concentration-dependent bronchodilation (P < 0.001 for either anesthetic; 40% +/- 11% [mean +/- SD] dilation for 3% isoflurane and 57% +/- 10% dilation for 3% halothane). For both anesthetics, bronchodilation was significantly but incompletely attenuated by epithelial rubbing (12% +/- 7% dilation for 3% isoflurane [P < 0.01] and 31% +/- 10% dilation for 3% halothane [P < 0.01]), by pretreatment with indomethacin (20% +/- 8% dilation for 3% isoflurane [P < 0.02] and 21% +/- 9% dilation for 3% halothane [P < 0.001]), or by L-NNA (9% +/- 7% dilation for 3% isoflurane [P < 0.005] and 39% +/- 12% dilation for 3% halothane [P < 0.05]). Epithelial rubbing did not impair nitroprusside-associated bronchodilation. CONCLUSIONS: Isoflurane- and halothane-mediated bronchodilation depends at least partially on the epithelium and may involve both a prostanoid and nitric oxide in distal rat bronchi.

Anesthetics, Inhalation↗
PubMed1997

Attitude adjustment.

How can you motivate physicians so that their decisions and behavior reflect what is best for the group practice, instead of themselves or their department? By clearly stating expectations and goals, physicians can learn that the priority must be the success of the group practice. Presented here is an example of how the Orlando Health Care Group (OHCG), a primary care medical group with 85 physicians in four specialties, addressed this challenge and the physicians' positive response to the change. To survive as a group, the OHCG had to abandon old ways of managing conflict and agree upon a list of core values around which it could evaluate all future physician behavior. The list became known as the "10 Commandments." They were meant to give every individual a sense of place and purpose within the group, knowing that the best way for an individual to prosper was to be part of a successful group.

Attitude of Health Personnel↗
PubMed1996

Steady-state myogenic response of rat coronary microvessels is preserved by isoflurane but not by halothane.

The myogenic response of vascular smooth muscle produces vasomotion in response to changes in vessel transmural pressure. While this is an important determinant of coronary blood distribution, the effect of volatile anesthetics on the response has not been previously investigated. In this study, we examined the effect of isoflurane and halothane on this myogenic response. Coronary resistance arteries were isolated from Wistar rats. As the intraluminal pressure was increased from 10 to 120 mm Hg in the presence of either isoflurane (1%, 2%, and 3%), halothane (1% and 2%), or no volatile agent (control), the vessel intraluminal diameter was monitored using a video detection system. Passive changes in vessel diameter were measured after exposure to papaverine 100 microM. Additionally, the myogenic responses of endothelium-intact and endothelium-denuded vessels were compared. Endothelium-intact control vessels demonstrated myogenic constriction above 80 mm Hg of intraluminal pressure. This response was not affected by endothelial denudation. The response was preserved by isoflurane 1%, 2% or 3% but abolished by halothane 1% or 2%. We conclude that, in rat coronary resistance arteries, myogenic constriction can be demonstrated above 80 mm Hg of intraluminal pressure and is endothelium independent. This response is preserved by isoflurane but abolished by halothane. These findings may have implications for the effect of the anesthetics on coronary blood flow distribution.

Anesthetics, Inhalation↗
PubMed1996

Protein kinase C-induced contraction is inhibited by halothane but enhanced by isoflurane in rat coronary arteries.

Protein kinase C (PKC), important in signal transduction, may help generate and maintain vascular smooth muscle tone. We sought to examine the effect of the volatile anesthetics isoflurane and halothane on PKC agonist-induced vasoconstriction and PKC inhibitor-induced vasorelaxation. Subepicardial resistance arteries were dissected from rat hearts. Changes in vessel diameters were monitored in response to the membrane-bound PKC agonist 12-deoxyphorbol-13-isobutyric-20-acetate (PBE) 10(-8)-10(-7) M or the cytosolic PKC agonist oleic acid 10(-7)-10(-5.5) M either in the presence of isoflurane 1.15%, isoflurane 2.3%, halothane 0.77%, halothane 1.54%, or no volatile anesthetics (control). In addition, after preconstriction with the thromboxane analog U46619 1 microM, relaxation responses to the PKC inhibitor staurosporine 10(-8)-10(-7) M were examined in the presence or absence of the anesthetics as above. PBE-induced constriction was attenuated by either concentration of halothane (P < 0.05) but was unaltered by isoflurane (P > 0.5). Oleic acid-induced constriction was abolished by halothane (P < 0.001) but enhanced by isoflurane (P < 0.01). Staurosporine-induced relaxation of U46619-preconstricted vessels was attenuated by isoflurane (P < 0.05) but unaltered by halothane (P > 0.3). We conclude that isoflurane may enhance cytosolic PKC-mediated vasoconstriction, whereas halothane may attenuate both cytosolic and membrane-bound PKC-mediated vasoconstriction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Cardiac risk of noncardiac surgery in patients with asymmetric septal hypertrophy.

BACKGROUND: Many data are available regarding cardiac risk in patients with coronary artery disease undergoing noncardiac surgery, but few data are available regarding risk for patients with hypertrophic cardiomyopathy and asymmetric septal hypertrophy. METHODS: Seventy-seven patients with asymmetric septal hypertrophy were identified in whom an echocardiogram had been performed within 24 months of noncardiac surgery. Patients' charts were reviewed for data regarding surgical operations, including length of surgery, type of anesthesia, and intravascular monitoring used. Data regarding adverse perioperative cardiac events also were gathered. RESULTS: Forty percent (n = 31) of patients had one or more adverse perioperative cardiac events, including one patient who had a myocardial infarction and ventricular tachycardia that required emergent cardioversion. There were no perioperative deaths. All 31 patients had minor outcomes. Of the 77 patients, perioperative congestive heart failure developed in 12 (16%). Factors associated with adverse cardiac events were increasing length of surgical time (P < 0.01) major surgery (P < 0.05), and intensity of monitoring (P < 0.05). Age, gender, resting outflow tract gradient, systolic anterior motion of the anterior mitral leaflet, prior myocardial infarction, severity of mitral regurgitation, type of anesthetic, septal thickness, and the interval between echocardiogram and surgery were not associated with the occurrence of adverse cardiac events. CONCLUSION: Patients with asymmetric septal hypertrophy undergoing noncardiac surgery have a high incidence of adverse cardiac events, frequently manifested as congestive heart failure. However, irreversible cardiac morbidity and mortality was extremely low. Important independent risk factors for adverse outcome in all patients include major surgery and increasing duration of surgery.

Adult↗